I. Field of the Invention
This invention relates generally to implantable cardiac rhythm management apparatus, and more particularly to such an apparatus and method that automatically establishes an optimum A-V delay interval for a DDD pacemaker.
II. Discussion of the Prior Art
With present day state-of-the-art, programmable, implantable pacemakers, a cardiologist is able to periodically program into the device an A-V delay value that yields an optimum stroke volume by, for example, using external instrumentation like a Doppler flow meter to measure changes in cardiac output as the A-V delay interval for the pacer is systematically changed. Such an approach at optimization is not only time consuming, but may only be appropriate for the patient at the time that the testing and setting of the A-V delay interval is made. In the literature, the optimum value of the A-V delay has generally been defined as that delay value that produces the maximum stroke volume for a fixed heart rate or the maximum cardiac output for a sinus node driven heart rate. For patients suffering from congestive heart failure (CHF), the A-V delay interval can be varied over a wide range without any measurable change in stroke volume. Studies which we have conducted suggest that CHF patients would have a very narrow range for the optimum A-V delay, meaning that small deviations, e.g., only 10 milliseconds, from the optimum can diminish the clinical benefit obtained using DDD pacing.
To explain these apparently contradictory results, one needs to understand that the body regulates the heart directly, such as by changing the heart rate and contractility, through the sympathetic and parasympathetic tones and indirectly through the load. A major role in this regulatory scheme is played by the baroreceptors. The baroreceptors, located in the major thoracic arteries, are pressoreceptors that compare the arterial pressure with a reference value. If the pressure exceeds the reference value, the baroreceptors emit signals that enter the tractus solitarius of the medulla. Secondary signals also inhibit the vasoconstrictor center of the medulla and excite the vagal center. The net effects are vasodilation of the veins and the arterioles throughout the peripheral circulatory system and decreased heart rate and strength of heart contractions. Therefore, excitation of the baroreceptors by pressure in the arteries reflexly causes the arterial pressure to decrease because of both a decrease in peripheral resistance and a decrease in cardiac output. Conversely, low pressure (a pressure lower than the reference value) has opposite effects, reflexly causing the pressure to rise back toward normal.
When it is recognized that A-V delay only effects the timing of the atrial contraction in relationship with the next following ventricular contraction, a change in A-V delay will only change the hemodynamic performance of the heart as a mechanical pump. If a patient is not already using his/her compensation mechanisms, a less than optimal A-V delay would mechanically impair the pump performance. If this impairment is of a sufficient degree to produce a pressure change, the baroreceptor mechanism can come into play to increase the contractility and cancel the hemodynamic effect that the less than optimum A-V delay would have produced. The more seriously that the heart of a CHF patient is impaired, the more his/her organism will use these compensation mechanisms and the less his/her regulatory system will be able to compensate for a less than optimum A-V delay. This tends to explain the finding of very narrow ranges of optimum A-V delays in sick patients.
In 1981, M. Heilman and M. Mirowski proposed a method and apparatus for maximizing stroke volume through atrioventricular pacing using an implanted cardioverter/pacer which accomplishes A-V sequential pacing with an A-V delay tailored to the particular patient. One of its disadvantages is that it attempted to control the A-V delay on a beat-by-beat basis, measuring the beat-by-beat stroke volume. However, the beat-by-beat variation of the peak-to-peak impedance proved not to be a reliable enough approach to be used as a parameter to determine the A-V delay, since its amplitude is going to be affected by motion artifacts, electric noise, etc. Another disadvantage of that method and apparatus is that it does not provide any way to identify the origin of the stroke volume change, which could have been produced by a change in heart rate, by a change in the systemic or peripheral resistance or by a change in the venous return. Also, any affect of the A-V delay on the stroke volume tends to be masked by physiologic feedback mechanisms that try to maintain cardiac output constant so as to satisfy metabolic needs.
We hypothesize that the clinical findings, obtained while using stroke volume as the variable to optimize A-V delay, have been affected by the feedback mechanisms that the body normally applies to maintain the supply of blood during load changes. If this hypothesis is correct, the A-V delay changes operate to modify the pump performance, but its actual output has been kept constant by the feedback introduced by the sympathetic and parasympathetic systems. In patients with a very narrow range for the optimum A-V delay, it is possible that their feedback mechanisms were either impaired or already used and, therefore, unable to completely compensate for the effect produced in the pump efficiency by the A-V delay.